scholarly journals Comparison of sarcolemmal calcium channel current in rabbit and rat ventricular myocytes.

1996 ◽  
Vol 493 (3) ◽  
pp. 733-746 ◽  
Author(s):  
W Yuan ◽  
K S Ginsburg ◽  
D M Bers
Keyword(s):  
Calcium Channel ◽  
Ventricular Myocytes ◽  
Rat Ventricular Myocytes ◽  
Channel Current

Changes of action potential and L-type calcium channel current of Sprague–Dawley rat ventricular myocytes by different amlodipine isomers

2008 ◽  
Vol 86 (9) ◽  
pp. 620-625 ◽  
Author(s):  
Ru-xing Wang ◽  
Wen-ping Jiang
Keyword(s):  
Steady State ◽  
Action Potential ◽  
Calcium Channel ◽  
Ventricular Myocytes ◽  
Channel Blockers ◽  
Sprague Dawley ◽  
Patch Clamp Technique ◽  
Rat Ventricular Myocytes ◽  
Channel Current ◽  
Steady State Inactivation

To investigate the effects of S- and R-amlodipine (Aml) on action potential (AP) and L-type calcium channel current (ICa-L), the whole-cell patch-clamp technique was used on rat ventricular myocytes to record AP, ICa-L, peak currents, steady-state activation currents, steady-state inactivation currents, and recovery currents from inactivation with S-Aml and R-Aml at various concentrations. Increasing concentrations of S-Aml gradually shortened AP durations (APDs). At concentrations of 0.1, 0.5, 1, 5, and 10 μmol/L, S-Aml blocked 1.5% ± 0.2%, 25.4% ± 5.3%, 65.2% ± 7.3%, 78.4% ± 8.1%, and 94.2% ± 5.0% of ICa-L, respectively (p < 0.05), and the half-inhibited concentration was 0.62 ± 0.12 µmol/L. Current–voltage curves were shifted upward; steady-state activation and inactivation curves were shifted to the left. At these concentrations of S-Aml, the half-activation voltages were –16.01 ± 1.65, –17.61 ± 1.60, –20.17 ± 1.46, –21.87 ± 1.69, and –24.09 ± 1.87 mV, respectively, and the slope factors were increased (p < 0.05). The half-inactivation voltages were –27.16 ± 4.48, –28.69 ± 4.52, –31.19 ± 4.17, –32.63 ± 4.34, and –35.16 ± 4.46 mV, respectively, and the slope factors were increased (p < 0.05). The recovery times from inactivation of S-Aml were prolonged (p < 0.05). In contrast, R-Aml had no effect on AP and ICa-L (p > 0.05) at the concentrations tested. Thus, only S-Aml has calcium channel blockade activity, whereas R-Aml has none of the pharmacologic actions associated with calcium channel blockers.

scholarly journals Hyposmotic challenge modulates function of L-type calcium channel in rat ventricular myocytes through protein kinase C

2010 ◽  
Vol 31 (11) ◽  
pp. 1438-1446 ◽  
Author(s):  
An-tao Luo ◽  
Hong-yan Luo ◽  
Xin-wu Hu ◽  
Lin-lin Gao ◽  
Hua-min Liang ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Calcium Channel ◽  
Ventricular Myocytes ◽  
Rat Ventricular Myocytes ◽  
Kinase C

scholarly journals Effects of Leonurine on L-Type Calcium Channel in Rat Ventricular Myocytes

2012 ◽  
Vol 35 (8) ◽  
pp. 1249-1256 ◽  
Author(s):  
Hong Xin ◽  
Ming Gu ◽  
Wen Wei Wang ◽  
Shi Ying Huang ◽  
Fang Ping Li ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Ventricular Myocytes ◽  
Rat Ventricular Myocytes

Effects of ropivacaine on membrane potential and voltage-dependent calcium channel current in single guinea-pig ventricular myocytes

2002 ◽  
Vol 16 (4) ◽  
pp. 273-278 ◽  
Author(s):  
Noboru Hatakeyama ◽  
Masana Yamada ◽  
Nobuko Shibuya ◽  
Mitsuaki Yamazaki ◽  
Shigeo Yamamura ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Guinea Pig ◽  
Calcium Channel ◽  
Ventricular Myocytes ◽  
Channel Current ◽  
Voltage Dependent Calcium Channel ◽  
Voltage Dependent

Inhibition of L-Type Ca2+Channel Current in Rat Ventricular Myocytes by Terfenadine

1997 ◽  
Vol 81 (2) ◽  
pp. 202-210 ◽  
Author(s):  
Shi Liu ◽  
Russell B. Melchert ◽  
Richard H. Kennedy
Keyword(s):  
Ventricular Myocytes ◽  
Rat Ventricular Myocytes ◽  
Channel Current

Gonadectomy of adult male rats reduces contractility of isolated cardiac myocytes

2003 ◽  
Vol 285 (3) ◽  
pp. E449-E453 ◽  
Author(s):  
Kish L. Golden ◽  
James D. Marsh ◽  
Yang Jiang ◽  
Tiane Brown ◽  
Jerome Moulden
Keyword(s):  
Cardiac Function ◽  
Calcium Channel ◽  
Cardiac Myocytes ◽  
Ventricular Myocytes ◽  
Functional Expression ◽  
Receptor Expression ◽  
Male Rats ◽  
Rat Ventricular Myocytes ◽  
Time To Peak ◽  
Isolated Rat

Sex-related differences in cardiac function have been well documented. The extent to which sex hormones are responsible for these differences is unclear. The current study was designed to determine whether castration and androgen replacement resulted in changes in functional expression of genes encoding the L-type calcium channel and Na/Ca exchanger in isolated rat ventricular myocytes. Sixteen weeks of castration produced a 50% decline in dihydropyridine receptor expression levels and a 16% ( P < 0.05) increase in time to peak shortening. Furthermore, cardiac myocytes isolated from castrated animals also displayed an 18% ( P < 0.001) increase in time to relengthening and an 80% decrease in Na/Ca exchanger gene expression when compared with intact controls. Testosterone treatment of castrated animals completely reversed these effects. These results provide the first evidence that androgens regulate functional expression of the L-type calcium channel and the Na/Ca exchanger in isolated rat ventricular myocytes and thus may play a role in modulating cardiac performance in males and thereby contribute to the observed gender differences in cardiac function.

BAY K 8644 modifies Ca2+cross signaling between DHP and ryanodine receptors in rat ventricular myocytes

1999 ◽  
Vol 276 (4) ◽  
pp. H1178-H1189 ◽  
Author(s):  
Satomi Adachi-Akahane ◽  
Lars Cleemann ◽  
Martin Morad
Keyword(s):  
Amplification Factor ◽  
Ventricular Myocytes ◽  
Ryanodine Receptors ◽  
Bay K 8644 ◽  
Local Exchange ◽  
Rat Ventricular Myocytes ◽  
Channel Current ◽  
Dependent Inactivation ◽  
Intracellular Ca ◽  
Kinetics Of

The amplification factor of dihydropyridine (DHP)/ryanodine receptors was defined as the amount of Ca2+ released from the sarcoplasmic reticulum (SR) relative to the influx of Ca2+ through L-type Ca2+ channels in rat ventricular myocytes. The amplification factor showed steep voltage dependence at potentials negative to −10 mV but was less dependent on voltage at potentials positive to this value. In cells dialyzed with 0.2 mM cAMP in addition to 2 mM fura 2, the Ca2+-channel agonist (−)-BAY K 8644 enhanced Ca2+-channel current ( I Ca), shifted the activation curve by −10 mV, and significantly delayed its inactivation. Surprisingly, BAY K 8644 reduced the amplification factor by 50% at all potentials, even though the caffeine-releasable Ca2+ stores were mostly intact at holding potentials of −90 mV. In contrast, brief elevation of extracellular Ca2+ activity from 2 to 10 mM enhanced both I Ca and intracellular Ca2+ transients in the absence or presence of BAY K 8644 but had no significant effect on the amplification factor. BAY K 8644 abolished the direct dependence of the rate of inactivation of I Ca on the release of Ca2+ from the SR. These findings suggest that the gain of the Ca2+-induced Ca2+ release in cardiac myocytes is regulated by the gating kinetics of cardiac L-type Ca2+ channels via local exchange of Ca2+ signals between DHP and ryanodine receptors and that BAY K 8644 suppresses the amplification factor through attenuation of the Ca2+-dependent inactivation of Ca2+ channels.

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